MANAGEMENT OF HEAD INJURY IN THE ITU

Chris Marshall SpR Anaesthetics

Plan

      Introduction Classification Pathophysiology Transfer Factors influencing outcome Additional monitoring and management

Introduction 1

    1 million a year in UK Mostly minor GCS 13-15, or moderate GCS 9-12.

Half<16yrs old.

Age distribution Bimodal comprising young people (15-29) involved in RTA’s and elderly folk in domestic accidents.

Introduction 2

    RTA’s responsible for 50% of all head injuries in UK Males 2-3 x more likely than females Associated with tremendous mortality and morbidity 1% of all deaths attributable to head injury

Introduction 3

  85% of all severely head injured patients remain disabled after 1 year and only 15% have returned to work at 5yrs.

Evan after apparently mild head injury, 50% of patients have moderate or severe disability 1yr later and only 45% return to full functional activity.

Classification

   By Nature of insult; penetrating or blunt.

Concomitant injuries; isolated head injury or multiple trauma.

Timing of the injury; Primary or Secondary.

Classification 2

  Primary injury is that occurring at the scene and is usually outside the control of the intensivist.

Secondary injury is anything that occurs to augment the primary injury; the prevention of this is predominantly where intensive therapy is aimed.

Glasgow Coma Score

  E4,V5,M6 Remains the most commonly used method of assessing the severity of a head injury; and although predictive of outcome, the motor part of the score has the greatest predictive ability.

Pathophysiology

     A range of pathological processes may be involved in a head injured patient.

Cerebral contusions Diffuse axonal injury Traumatic SAH Epidural or subdural haematoma.

Cerebral contusions 1

   Areas of ‘bruising’ within the brain with relatively localised cellular damage, haemorrhage and oedema.

These may be large haemorrhagic lesions or small point contusions.

The effects of these on outcome will depend on location and size along with pressure effects that they may generate locally

Cerebral contusions 2

 As with contusions elsewhere in the body, the associated maximum swelling and bleeding is often not seen until up to 72hrs after the initial insult.

Diffuse axonal injury

 Depicted by loss of grey/white differentiation on CT scan is caused by widespread shearing forces that occur as the brain undergoes stresses such as rapid deceleration.

Traumatic SAH

 Bleeding associated with tearing of an intracranial vessel by the shaking of brain tissue in a traumatic situation.

SAH

 As for non-traumatic SAH, traumatic SAH may be associated with vasospasm. Evidence for the beneficial effects of Nimodipine in this setting has been limited by poor quality studies, and it cannot be recommended unless vasospasm has been demonstrated by angiography or alternative imaging techniques.

Epidural or sub-dural haematoma

  Occur frequently after trauma and if bilateral, the associated localising signs may be absent.

May have little underlying brain damage.

Epidural haematoma 2

  But if of sufficient size, brain compression and ischemia may occur.

Early evacuation is generally associated with a good outcome.

Sub-dural haematoma

  Much worse prognosis because of the involvement of underlying brain tissue.

Surgical evacuation will usually be performed if there is any evidence of mass effect or increased ICP to which the haematoma may be contributing.

Transfer of head injured patient

 To specialist neurosurgical centre if… Severe head injury or focal signs (whether or not they need neurosurgical intervention); and Needing ventilation, ICP monitoring or both.

Discuss fully, scans reviewed.

Transfer Checklist GCS<8

     Airway secured definitively Staff trained in airway and head injury Large bore i.v. access End-tidal CO2 maintained at 4-4.5kPa on transport ventilator SpO2 and art. gases checked for adequate oxygenation.

Transfer Checklist GCS<8

   Blood pressure adequate and fluids and vasopressors available Brain CT imaging complete and hard copies available Transfer complete within 4 hrs – no inappropriate delay

Factors influencing outcome

 Evidence base extremely limited, after full review of the literature, The Brain Trauma Foundation (BTF), in collaboration with the American Association of Neurological Surgeons, concluded that there are insufficient data to support a treatment standard or a treatment guideline for the initial management of the head injured patient.

Rapid physiological resuscitation



NORMOTENSION



NORMOXIA



NORMOCAPNIA



NORMOTHERMIA



NORMOGLYCAEMIA

NORMOTENSION

    Single episode of systolic BP < 90mmHg has a direct negative effect on outcome after traumatic brain injury.

Strenuous attempts should be made to maintain BP in the normal range.

Initially fluids then vasopressors.

NA most popular. MAP of at least 70 mmHg

NORMOXIA

  Hypoxemia (SpO2<90%) is associated with a worse outcome.

In one study there was approximately a four fold increase in mortality in patients with documented hypoxemia compared with non-hypoxemic patients.

NORMOXIA

 Maintenance of oxygenation needs to be balanced against the CVS effects of additional PEEP in patients with combined head and chest trauma, a compromise may have to be reached to provide the best quality conditions for the brain, potentially at the expense of a protective lung strategy

NORMOCAPNIA

  Hyperventilation (PaCO2<25mmHg) should be specifically avoided in the first 24hrs after traumatic brain injury and should not be a target for prolonged ventilation.

Hyperventilation results in cerebral vasoconstriction and a subsequent decrease in CBF.

NORMOCAPNIA

 In the first 24hrs after head injury CBF is reduced to approximately half that of normal, and aggressive hyperventilation may result in further cerebral ischemia.

NORMOTHERMIA

  An increase in body and brain temperature is associated with an increase in CBF, cerebral metabolic requirement for oxygen and oxygen utilisation, resulting in an increase in ICP and further cerebral ischaemia.

Pharmacological antipyretics and surface cooling.

NORMOGLYCAEMIA

   Brain is an obligate glucose user Hyperglycaemia is associated with an increase in cerebral metabolism; because of decreased CBF subsequent to trauma this results in additional anaerobic metabolism.

Therefore use insulin to keep blood glucose in the range 4-8mmolL

ADDITIONAL MONITORING

    All above in any ICU.

Why need more?

To guide the timing of repeat scans and neurosurgical intervention.

Benefits in terms of morbidity and mortality unclear at present.

ICP monitoring

  BTF suggest insufficient data to make this a treatment standard, but suggest ICP monitoring is appropriate in patients with severe head injury with an abnormal admission CT scan. An abnormal CT scan of the head is one which reveals haematomas, contusions, oedema or compressed basal cisterns.

ICP monitoring

    Guide therapy to limit rise in ICP Allow calculation and maintenance of CPP Patients with a severe head injury and a high ICP have a poorer prognosis than those with a normal ICP.

Critical ICP at which to take action is not clear but is between 15-30mmHg. 20mmHg widely accepted and treatment protocols based on this figure.

Cerebral perfusion pressure

CPP=MAP-ICP

ICP

   Measurement never subjected to RCT V difficult to do so Probably helps in early detection of mass lesions, may limit the indiscriminate use of therapies to control ICP (which may themselves be harmful) and may be helpful in determining prognosis.

Measurement of ICP

    Various sites, various devices.

Intraparenchymal/intraventricular catheter/Subdural or epidural.

Infection/CSF aspiration Right frontal lobe preferred as non dominant hemisphere and minimal essential brain tissue.

Alternative protocols

    CPP management ROSNER, 1995, 158 patients severe traumatic brain injury were managed with vasopressors (NA + phenylephrine) to maintain CPP>70mmHg.

Outcome compared to standard ICP based management protocol patients collected from Traumatic Coma Data Bank.

In all GCS categories M + M Improved.

NO RCT’s

Alternative protocols

  LUND 1998 suggested that high CPP management may have adverse effects of triggering vasogenic brain oedema leading to raised ICP and therefore counteracting desired increase in CPP.

Jugular bulb oxyhaemaglobin saturation protocol

Management of raised ICP

   The higher the icp the worse the outcome BTF suggest maintaining ICP<20mmHg Medical and Surgical strategies are employed to achieve this.

Medical

      Positioning Sedation and neuromuscular block Ventilation and CO2 control Mannitol and Osmolality management Seizure control Temperature control and induced hypothermia

Positioning

  Nursed 30 degree head up.

Must be certain of integrity of spine.

Sedation and NMB

   Deep sedation is used to reduce cerebral metabolism. (Ramsay score<6) Some units routinely use NMBD’s others only if ICP remains high despite all other medical measures in place.

Thiopentone + EEG to achieve burst suppression.

Ventilation and CO2 control

  4-4.5kPa

If ICP becomes dramatically increased short term hyperventilation may be used to gain control whilst other measures are implemented.

Mannitol and osmolality management

  An increase in serum osmolality will result in a tendency to decrease brain tissue water and hence ICP.

Target 300-310mosm, achieved by incremental doses of 100ml mannitol 20%

Seizure control

  Prevent them.

If NMBD’s employed EEG should also be used.

Temperature control.

  Avoid increase in temp.

Decrease contentious.

Surgical

   CSF Drainage Craniectomy Lobectomy/Removal of contusion.

Summary

   Put your seat-belt on Slow down Wear a helmet, even if you’re in a car.